Transdermal nicotine modulates strategy-based attentional semantic processing in non-smokers.

 was found to selectively affect priming condition reaction times at the long SOA, indicating a 

Pharmacological chaperoning of nAChRs: a therapeutic target for Parkinson's disease.

At the subcellular level, pharmacological chaperoning by

 ligands causes profound changes in the structure and function of the endoplasmic reticulum (ER), ER exit sites, the Golgi apparatus and secretory vesicles of cells.

Local Delivery of Nicotine does not Mitigate Fibrosis but may Lead to Angiogenesis

 agonists inhibit inflammatory signaling.

Prenatal nicotine exposure increases GABA signaling and mucin expression in airway epithelium.

 to increase mucin expression was blocked by 

Nicotinic receptors in aging and dementia.

 agonists have been shown to improve cognitive function in aged or impaired subjects.

Cognitive effects of nicotine

 agonists have been found to improve performance on attention and memory tasks.

Prenatal nicotine alters vigilance states and AchR gene expression in the neonatal rat: implications for SIDS.

 and muscarinic cholinergic receptor mRNAs in brain regions involved in regulating vigilance states.

Contribution of CNS nicotine metabolites to the neuropharmacological effects of nicotine and tobacco smoking.

 subtype diversity increases the complexity of the potential mechanisms of action of 

Maintenance of behavior by postponement of scheduled injections of nicotine in squirrel monkeys.

 antagonist with both central and peripheral effects, shifted the 

 dose-response curve to the right by about 1 log unit and blocked nicotine-induced emesis.

Nicotine protects against manganese and iron-induced toxicity in SH-SY5Y cells: Implication for Parkinson's disease

 effects, in turn were blocked by selective 

Nerve gas antidotes.

 is a convulsant poison,3,4 and nerve agents enhance 

 depolarizations5 and modulate nicotinic receptor ion channels directly by an allosteric effect6,7—as does pyridostigmine,8 which is used as a protective measure against nerve gases.

Primary reinforcement in the maintenance of cigarette smoking

 antagonists to block primary reinforcement and hasten extinction of conditioned reinforcement is also considered.

Chronic Nicotine Exposure Alters the Neurophysiology of Habenulo-Interpeduncular Circuitry

Together, these results indicate that chronic exposure to

 cholinergic signaling and cell excitability in Hb-IP circuits, a key pathway involved in nicotine dependence.

Involvement of Nicotinic Receptor Subtypes in the Behavioral Effects of Nicotinic Drugs in Squirrel Monkeys

 were antagonized by mecamylamine (nonselective), not appreciably altered by dihydro-β-erythroidine (α4β2 selective), and exacerbated by the 

 partial agonists, varenicline and cytisine.

Mutually augmenting interactions of dextromethorphan and sazetidine-A for reducing nicotine self-administration in rats

 drug treatments have been found to decrease 

Early postnatal nicotine exposure causes hippocampus-dependent memory impairments in adolescent mice: Association with altered nicotinic cholinergic modulation of LTP, but not impaired LTP

 modulation of CA1 activity: activation of nicotinic receptors no longer increases CA1 network depolarization, acute nicotine inhibits rather than facilitates the induction … the SC pathway by recruiting an additional nicotinic receptor subtype, and acute nicotine no longer blocks LTP induction at the temporoammonic pathway.

 cholinergic-dependent plasticity is required for long-term memory formation and that postnatal 

 exposure disrupts this form of plasticity.

Investigation of NADH Binding, Hydride Transfer, and NAD+ Dissociation during NADH Oxidation by Mitochondrial Complex I Using Modified Nicotinamide Nucleotides

 fragments that lack the adenosine do not bind, and ADP-ribose binds more strongly than NAD+, suggesting that the 

Nicotine blocks ethanol-induced apoptosis in primary cultures of rat cerebral cortical and cerebellar granule cells

 in this model may be suggestive of potential use of 

 agonists in neurotoxic insults and/or neu-rodegenerative disorders.

Nicotine inhibits ethanol-induced toxicity in cultured cerebral cortical cells

 antagonists such as mecamylamine (1-20 μM), dihydro-beta-erythroidine (DHBE) (50 nM-1.0 μM) and methyllycaconitine (MLA) (5 nM-1 μM) in a dose-dependent manner.

Protective effects of nicotine on ethanol-induced toxicity in cultured cerebellar granule cells

 antagonists such as mecamylamine 1–20 μM, dihydro-β-erythroidine 1.0 nM–1.0 μM and methyllycaconitine 5 nM-5 μM in a dose-dependent manner.

 antagonists, implicating both high and low affinity nicotinic receptors in mediating the actions of nicotine.

Responses of limbic and extrapyramidal substance P systems to nicotine treatment

ConclusionsThese findings indicate that some limbic and basal ganglia SP systems are significantly affected by exposure to

 and dopaminergic receptors, suggesting a role for SP pathways in nicotine’s limbic and extrapyramidal effects.

Chronic nicotine and dizocilpine effects on regionally specific nicotinic and NMDA glutamate receptor binding

Antinociceptive effects of central and systemic administrations of nicotine in the rat

 or muscarinic blockers implicating both classes of cholinergic receptors in this effect.

Possible explanations for the antagonism by nicotine against reserpine-induced depletion of monoamines in mouse brain

These results suggest that inhibitory effect of nicotine on the intraperitoneal reserpine-induced depletion of brain monoamines is due to an inhibition of absorption of reserpine, and that

 of reserpine-induced dopamine depletion.

Reversal of a Vigilance Decrement in the Aged Rat by Subtype-Selective Nicotinic Ligands

 has been demonstrated to improve both normal and disordered attention, suggesting potential clinical utility for 

Neurobehavioural defects in adult mice neonatally exposed to nicotine: changes in nicotine-induced behaviour and maze learning performance

Furthermore, it was shown that in mice exposed neonatally to a

 dose known to inhibit the development of the 

 low affinity-binding site (LA), the response to nicotine could not cause any increase in spontaneous motor activity as seen in controls.

Influence of Various Drugs on the Voluntary Intake of Nicotine by Rats

 and dopaminergic D4 receptors partially reduce the desired effect of 

 by forcing the animals to consume more of this substance.

Involvement of adrenergic and cholinergic systems in nicotine-induced anxiogenesis in mice.

It can be concluded that certain doses of

 (0.25 and 0.5 mg/kg) 7 min after their injection induce an anxiogenic effect through 

 mechanism(s), and that involvement of alpha(1)- but not alpha(2)-adrenoceptors in the response to nicotine seems likely.

Differential agonist inhibition identifies multiple epibatidine binding sites in mouse brain.

However, inhibition of epibatidine binding by

, acetylcholine, methylcarbachol and cytisine in olfactory bulbs revealed a biphasic pattern consistent with the presence of two sites differentially sensitive to inhibition by these 

Selective α7-nicotinic agonists normalize inhibition of auditory response in DBA mice

 agonists produce brief periods of normal sensory inhibition in these mice.

Alteration of brain nicotinic receptors induced by immobilization stress and nicotine in rats

However, chronic nicotine treatment abrogated stress induced downregulation of the [3H]cytisine binding sites, suggesting that

Inhibition by dizocilpine (MK‐801) of striatal dopamine release induced by MPTP and MPP+: possible action at the dopamine transporter

 antagonists, mecamylamine and chlorisondamine, and by MK‐801 (all at 100 μm); K+‐evoked release was not affected.

Place preference conditioning with ventral tegmental injections of cytisine.

These findings provide additional evidence in support of the hypothesis that

 actions at the level of the ventral tegmentum contribute to the reinforcing actions of systemic injections of 

Chronic nicotine exposure enhances cutaneous axon reflexes in the rat.

 cholinoceptors on skin nociceptors and primary afferents upregulate in response to 

 exposure, and return to normal following nicotine cessation.

Development of fast synaptic transmission in bullfrog sympathetic ganglia.

 synapses was demonstrated by reversible blockade in low Ca2+, high Mg2+ Ringer and in 

Existence of different subtypes of nicotinic acetylcholine receptors in the rat habenulo-interpeduncular system

 agonists decreased the amplitude of the afferent volley with different efficacies: 

 greater than cytisine greater than ACh greater than DMPP.

Regulation of the secretory response in bovine chromaffin cells.

 current was rapid, with time constants of 22 and 155 ms at 10 microM 

Nicotinic Modulation of [3H]Dopamine Release from Striatal Synaptosomes: Pharmacological Characterisation

, cytisine, and DMPP were inhibited by low concentrations of the 

 antagonists dihydro‐β‐erythroidine, mecamylamine, pempidine, and neosurugatoxin; α‐bungarotoxin was without effect, and extending the time of exposure to this toxin resulted in only very modest inhibition.

Effect of Chronic Nicotine Treatment on Nicotinic Autoreceptor Function and N‐[3H]Methylcarbamylcholine Binding Sites in the Rat Brain

 ([3H]MCC) binding site density in the frontal cortex, hippocampus, and striatum and results in the loss of nicotinic receptor‐mediated positive feedback in the cortex and hippocampus.

Behavioral effects of acute hexamethonium in rats chronically intoxicated with nicotine

These data show that predominantly peripheral

 blockade can partially alleviate the effects of 

 administration of feeding behavior, suggesting that at least some of the effects of nicotine on feeding are peripheral.

Heterogeneity of nicotine actions in the rat cerebellum: an in vivo electrophysiologic study.

The effects of nicotine on cell discharge rate were probably receptor mediated because "classical" nondepolarizing

 antagonists selectively blocked the agonistic actions of 

Calcium Uptake and Catecholamine Secretion by Cultured Bovine Adrenal Medulla Cells

 antagonists block 45Ca2+ uptake induced by 

, tetrodotoxin blocks 45Ca2+ uptake induced by veratridine, and D600 blocks uptake induced by K+, nicotine, and veratridine, but not 45Ca2+ uptake or secretion induced by Ionomycin.

Characterization of cholinergic control of vasopressin release by the organ-cultured rat hypothalamo-neurohypophyseal system.

 antagonists, hexamethonium, tetraethylammonium chloride, and trimethaphan blocked VP release in response to acetylcholine and 

Long-term effects of early postnatal nicotine exposure on cholinergic function in the mouse hippocampal CA1 region

 exposure impairs both the induction and 

 modulation of NMDAR-dependent long-term depression (LTD).

The effect of varying hormonal and precursor supplementations on levels of nicotine and related alkaloids in cell cultures ofNicotiana tabacum

Feeding suspensions with amino acids either alone, or in combination with nicotinic acid and

The therapeutic potential of nicotine and nicotinic agonists for weight control.

 agonists may have a therapeutic potential for a variety of disorders, including Alzheimer's and Parkinson's diseases, depression, attention deficit disorder, Tourette's syndrome and ulcerative colitis.

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Possible Interaction: Niacin and Nicotine

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Research Papers that Mention the Interaction